Abstract

The cytokine hormone erythropoietin (EPO) and the chemokine CCL3 are known to be produced in the brain under various pathological conditions. In this study, we investigated whether EPO and CCL3 influence on each other during neuroinflammation. We showed that EPO could reduce lipopolysaccharide (LPS)-induced CCL3 mRNA expression in rat cerebellar neuron-enriched preparations (real-time RT–PCR). Whereas administration of EPO or CCL3 respectively mediated neuroprotective properties after LPS treatment, the combinations of both molecules resulted in increased caspase 3/7 activity. Thus, it seems that – probably depending on particular conditions – EPO and CCL3 may cancel each other's functional properties.

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